Atheroprotective effects of statins in patients with unstable angina by regulating the blood-borne microRNA network

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Abstract

Experimental studies have demonstrated several effects of statins in acute coronary syndrome (ACS) that may extend their clinical benefit beyond the lipid profile modification itself. However, the precise underlying mechanism remains to be elucidated. microRNAs (miRNAs) serve significant roles in the pathophysiology of atherosclerotic plaque progression. The present study investigated the protective role of statins in patients with unstable angina (UA) by regulating the circulating miRNA network. miRNA array results demonstrated that there were 21 differentially expressed miRNAs in non-statin-treated patients with UA (n=8) compared with non-coronary artery disease controls (n=8), and 33 differentially expressed miRNAs in statin-treated patients with UA (n=8) compared with non-statin patients. TargetScan and miRanda programs were used to predict miRNAs target genes. miRNAs target genes in vascular endothelial cells and monocytes were clustered based on the CGAP SAGE library via the Database for Annotation, Visualization and Integrated Discovery (DAVID) platform, and miRNA target genes in platelets were clustered based on a UP tissue-specific library via the DAVID platform. The PANTHER database via DAVID platform was used to perform signaling pathway analysis. The miRNA-gene/pathway network was visualized by Cytoscape software. Bioinformatic analysis suggested that statin-induced miRNAs functions were primarily enriched in angiogenesis, integrin and platelet derived growth factor signaling pathways in UA patients. In endothelial cells and platelets, statin-induced miRNAs primarily targeted the integrin signaling pathway, and in monocytes primarily targeted cytoskeletal regulation by the Rho GTPase signaling pathway. These results revealed that statins may serve systematic protective roles in UA patients by influencing the circulating miRNA regulatory network. Further studies are required to verify the functions of statin-induced miRNAs in endothelial cells, platelets and monocytes.

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Most cited references 35

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MicroRNAs and cancer: short RNAs go a long way.

Andrea Ventura, Tyler Jacks (2009)

MicroRNAs (miRNAs) may be important regulators of gene expression. By modulating oncogenic and tumor suppressor pathways they could, in principle, contribute to tumorigenesis. Consistent with this hypothesis, recurrent genetic and epigenetic alterations of individual miRNAs are found in some tumors. Functional studies are now elucidating the mechanism of action of putative oncogenic and tumor suppressor miRNAs.

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Effects of atorvastatin on early recurrent ischemic events in acute coronary syndromes: the MIRACL study: a randomized controlled trial.

G G Schwartz, A Olsson, M Ezekowitz … (2001)

Patients experience the highest rate of death and recurrent ischemic events during the early period after an acute coronary syndrome, but it is not known whether early initiation of treatment with a statin can reduce the occurrence of these early events. To determine whether treatment with atorvastatin, 80 mg/d, initiated 24 to 96 hours after an acute coronary syndrome, reduces death and nonfatal ischemic events. A randomized, double-blind trial conducted from May 1997 to September 1999, with follow-up through 16 weeks at 122 clinical centers in Europe, North America, South Africa, and Australasia. A total of 3086 adults aged 18 years or older with unstable angina or non-Q-wave acute myocardial infarction. Patients were stratified by center and randomly assigned to receive treatment with atorvastatin (80 mg/d) or matching placebo between 24 and 96 hours after hospital admission. Primary end point event defined as death, nonfatal acute myocardial infarction, cardiac arrest with resuscitation, or recurrent symptomatic myocardial ischemia with objective evidence and requiring emergency rehospitalization. A primary end point event occurred in 228 patients (14.8%) in the atorvastatin group and 269 patients (17.4%) in the placebo group (relative risk [RR], 0.84; 95% confidence interval [CI], 0.70-1.00; P =.048). There were no significant differences in risk of death, nonfatal myocardial infarction, or cardiac arrest between the atorvastatin group and the placebo group, although the atorvastatin group had a lower risk of symptomatic ischemia with objective evidence and requiring emergency rehospitalization (6.2% vs 8.4%; RR, 0.74; 95% CI, 0.57-0.95; P =.02). Likewise, there were no significant differences between the atorvastatin group and the placebo group in the incidence of secondary outcomes of coronary revascularization procedures, worsening heart failure, or worsening angina, although there were fewer strokes in the atorvastatin group than in the placebo group (12 vs 24 events; P =.045). In the atorvastatin group, mean low-density lipoprotein cholesterol level declined from 124 mg/dL (3.2 mmol/L) to 72 mg/dL (1.9 mmol/L). Abnormal liver transaminases (>3 times upper limit of normal) were more common in the atorvastatin group than in the placebo group (2.5% vs 0.6%; P<.001). For patients with acute coronary syndrome, lipid-lowering therapy with atorvastatin, 80 mg/d, reduces recurrent ischemic events in the first 16 weeks, mostly recurrent symptomatic ischemia requiring rehospitalization.

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Pathophysiology of native coronary, vein graft, and in-stent atherosclerosis.

Kazuyuki Yahagi, Frank Kolodgie, Fumiyuki Otsuka … (2016)

Plaque rupture, usually of a precursor lesion known as a 'vulnerable plaque' or 'thin-cap fibroatheroma', is the leading cause of thrombosis. Less-frequent aetiologies of coronary thrombosis are erosion, observed with greatest incidence in women aged <50 years, and eruptive calcified nodules, which are occasionally identified in older individuals. Various treatments for patients with coronary artery disease, such as CABG surgery and interventional therapies, have led to accelerated atherosclerosis. These processes occur within months to years, compared with the decades that it generally takes for native disease to develop. Morphological identifiers of accelerated atherosclerosis include macrophage-derived foam cells, intraplaque haemorrhage, and thin fibrous cap. Foam-cell infiltration can be observed within 1 year of a saphenous vein graft implantation, with subsequent necrotic core formation and rupture ensuing after 7 years in over one-third of patients. Neoatherosclerosis occurs early and with greater prevalence in drug-eluting stents than in bare-metal stents and, although rare, complications of late stent thrombosis from rupture are associated with high mortality. Comparison of lesion progression in native atherosclerotic disease, atherosclerosis in saphenous vein grafts, and in-stent neoatherosclerosis provides insight into the pathogenesis of atheroma formation in natural and iatrogenic settings.

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Author and article information

Journal

Journal ID (nlm-ta): Mol Med Rep

Journal ID (iso-abbrev): Mol Med Rep

Title: Molecular Medicine Reports

Publisher: D.A. Spandidos

ISSN (Print): 1791-2997

ISSN (Electronic): 1791-3004

Publication date (Print): January 2017

Publication date (Electronic): 24 May 2017

Publication date PMC-release: 24 May 2017

Volume: 16

Issue: 1

Pages: 817-827

Affiliations

[1 ]Department of Cardiology, Peking University People's Hospital, Beijing 100044, P.R. China

[2 ]Beijing Key Laboratory of Early Prediction and Intervention of Acute Myocardial Infarction and Center for Cardiovascular Translational Research, Peking University People's Hospital, Beijing 100044, P.R. China

[3 ]Center for Cardiovascular Translational Research, Peking University People's Hospital, Beijing 100044, P.R. China

[4 ]Department of Cardiology, Beijing Tiantan Hospital, Capital Medical University, Beijing 100050, P.R. China

Author notes

Correspondence to: Dr Hong Chen, Department of Cardiology, Peking University People's Hospital, 11 Xizhimen South Street, Xicheng, Beijing 100044, P.R. China, E-mail: chenhongbj@ 123456medmail.com.cn

Article

Publisher ID: mmr-16-01-0817

DOI: 10.3892/mmr.2017.6616

PMC ID: 5482202

PubMed ID: 28560417

SO-VID: 57cd84bc-b01b-4865-b449-1f6634799d0c

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This is an open access article distributed under the terms of the Creative Commons Attribution-NonCommercial-NoDerivs License, which permits use and distribution in any medium, provided the original work is properly cited, the use is non-commercial and no modifications or adaptations are made.

Atheroprotective effects of statins in patients with unstable angina by regulating the blood-borne microRNA network

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Most cited references 35

MicroRNAs and cancer: short RNAs go a long way.

Effects of atorvastatin on early recurrent ischemic events in acute coronary syndromes: the MIRACL study: a randomized controlled trial.

Pathophysiology of native coronary, vein graft, and in-stent atherosclerosis.

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